Potential influence of gut microbiota on the process of hypertriglyceridemia-aggravated acute pancreatitis

Abstract

Acute pancreatitis (AP) is sudden inflammation of the pancreas, which can lead to multiple organ dysfunction in severe cases. Hypertriglyceridemia (HTG) is the third most common cause. In recent years, HTG-induced AP (HTG-AP) has garnered increasing attention. Compared to AP caused by other causes, HTG-AP often has a more subtle onset but is more likely to progress to a severe, critical illness that poses a serious threat to a patient’s life and health. Research suggests a potential connection between the gut microbiota and AP, which could be mediated by bacterial metabolites, immune cells, and inflammatory factors. This is supported by observations of microbial imbalance and higher intestinal permeability in patients with AP. In addition, studies have shown that HTG-induced changes in gut microbiota can worsen AP by negatively impacting the host metabolism, immune response, and function of the intestinal barrier. In this review, we summarize recent clinical and animal studies on the role and mechanism of gut microbiota in the severity of AP aggravated by HTG. The application prospects of the newly proposed microbial-host-isozyme concept are summarized, focusing on its potential for the precision diagnosis and treatment of HTG-AP through gut microbiota regulation.

Keywords: Gut microbiota; Hypertriglyceridemia; Gut-pancreas axis; Acute pancreatitis; Microbial-host-isozyme

Core Tip: Current academic consensus is that hypertriglyceridemia (HTG) primarily exacerbates acute pancreatitis (AP) through lipotoxicity. This traditional view emphasizes that in HTG, pancreatic lipase in acinar cells hydrolyzes triglycerides, generating excessive free fatty acids, which exacerbates AP severity. However, recent evidence has increasingly demonstrated the critical role of the gut microbiota in this pathological process. This review explores how gut microbiota dysbiosis mediates the aggravation of AP caused by HTG, focusing on mechanisms such as microbial translocation, immune dysregulation, and metabolites. The novel “microbial-host-isozyme” concept is proposed for precise diagnosis and therapy in HTG-AP.